Summary
Dexamethasone (Dexa) has been commonly used in humans and domestic animals, particularly
in the treatment of tendon injuries and cartilage degeneration. However, it is often
associated with tendon rupture and impaired tendon and cartilage healing. In the present
study, we investigated Dexa’s in vitro effects on the growth of cell proliferation and the induction of apoptosis in canine
Achilles tendon cells and chondrocytes. Cell proliferation after treatment with Dexa
for two to six days was quantified by a 2,3-bis{2-methoxy- 4-nitro-5-sulfophenyl}-2H-tetrazolium-5-carboxyanilide
inner salt assay (XTT). The results showed that Dexa could inhibit the proliferation
of tendon cells and chondrocytes at increasing concentrations (0.1–50 μg/ml) compared
with untreated cells. Cell apoptosis was induced by Dexa, as evidenced by the typical
nuclear apoptosis using Hoechst 33258 staining. Dexa increased the apoptosis of canine
tendon cells and chondrocytes in a time-dependent manner. In canine tendon cells and
chondrocytes that were treated with 25 and 50 μg/ml concentration of Dexa, the number
of condensed apoptotic nuclei was significantly increased. In addition, culturing
with Dexa and the glucocorticoid receptor blocker, mifepristone, significantly arrested
apoptosis of tendon cells and chondrocytes. Based on our in vitro data, we hypothesized that in vivo treatment with glucocorticoids may diminish the proliferation of tendon and cartilage
cells by increasing apoptosis and suppressing the proliferation. Our findings suggest
that Dexa could be used with caution in dogs with articular or tendon problems.
Keywords
Dexamethasone - apoptosis - proliferation - canine tendon cells - chondrocytes
